Fig. 6

Schematic diagram summarizing the role of ECM, hypoxia, HIF-1α-dependent production of collagen type I (COL1), and integrins α2β1 and α11β1 in cell survival, proliferative potential, and stemness maintenance in DPSCs. In the absence of COL coating, upon reaching overconfluence, the multilayer formation generates the hypoxic environment, leading to apoptotic death accompanied by mitochondrial abnormality in the XFM cells. COL coating promotes cellular attachment, proliferation, and survival of COL-XFM cells. Furthermore, nuclear localization of HIF-1α within the COL-XFM multilayer activates the production of COL1. The resulting COL1-integrins α2β1/α11β1 interactions lead to cell survival and increased proliferative potential. Upon passaging, the COL-XFM cells retain stemness (i.e., proliferative ability, multidifferentiation potential, and stem cell phenotype) and chromosomal stability. Without COL coating, XFM cells display apoptosis and mitochondrial abnormality